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case

Itchy Lesions on the Back of the Leg

 

BACKGROUND

A 32-year-old man presents to the emergency department with an itchy and painful rash on the back of his left leg (see Image). About 7 days ago, he began to feel an “intense, burning” pain behind his left knee. Over the subsequent days, “small blisters” began to “pop up” over the area but were the worst behind the knee itself. He treated the lesion with an over-the-counter antibiotic ointment and acetaminophen (Tylenol), but they did not relieve the pain. Any contact, however slight, with the apparent blisters immediately intensifies the pain. The patient reports having fevers, sneezing, and a runny nose over the last 2 weeks. He does not report any cough, shortness of breath, headaches, or fatigue. He also reports extreme stress at work with many deadlines and an ongoing threat of job loss because of continuing downsizing due to overseas corporate operations. He denies exposing the affected area to heat or cold (burn) or to chemical agents, including detergents or cleaning agents. He has not started taking any new medications recently and is currently taking only acetaminophen. He has no known drug allergies, he quit smoking tobacco several years ago, and he drinks alcohol only rarely. His medical history is significant only for an appendectomy. On physical examination, the patient’s vital signs are a temperature of 37.2°C, a heart rate of 82 beats per minute, and a blood pressure of 124/67 mm Hg. Lesions are observed on the back of the left knee (see Image), and similar but smaller lesions appear in a bandlike distribution along the posterior length of his left leg up to the buttock region. The affected leg is neurovascularly intact. Remaining findings on neurologic examination, cardiorespiratory examination, and the review of systems are unremarkable.

 ***** HINT *****
Consider the intense, burning pain occurring in a bandlike distribution.

***** ANSWER *****

Herpes zoster (shingles): Herpes zoster is a viral infection caused by the varicella-zoster virus (VZV), the same virus that leads to chickenpox on initial exposure, which is usually in childhood. After the initial exposure and chickenpox resolves, the virus remains latent in the posterior spinal or cranial sensory ganglia for the person’s lifetime. Focal reactivation along the ganglial distribution in adulthood leads to herpes zoster. Factors responsible for reactivating the virus are not well delineated but may include depression of the immune system, trauma, advanced age, exposure to radiation, certain medications, infection, or stress. Most cases are relatively mild and occur along an isolated dermatomal distribution (see Image 2). Paresthesias or pain along the affected dermatome usually precede the disease. However, severe or complicated cases can also occur. For example, especially in immunocompromised patients, multidermatomal reactivation and dissemination can occur with hematogenous spread, bacterial superinfection leading to sepsis, or CNS and visceral involvement. Other specific complications such as meningoencephalitis, transverse myelitis, cranial-nerve palsies, granulomatous angiitis, hepatitis, and pneumonitis can also occur. Granulomatous angiitis may result in a cerebrovascular accident. In addition, reactivation along the ophthalmic division of the trigeminal nerve can lead to ocular involvement and herpes zoster ophthalmicus with a resultant risk for conjunctivitis, keratitis, corneal ulceration, iridocyclitis, glaucoma, and blindness. Involvement of the nasociliary branch often appears as a single lesion on the tip of the nose (ie, Hutchinson sign). Failure to perform slit-lamp examination with fluorescein stain to identify the dendritic corneal lesions may lead to a missed diagnosis of herpetic zoster ophthalmicus. Involvement of the geniculate ganglion can produce Ramsay Hunt syndrome or herpes zoster oticus. This involvement is characterized by pain in the external ear, external auditory canal, and tympanic membrane. Transient, unilateral facial paralysis is not uncommon. Ramsay Hunt syndrome can be associated with vertigo, tinnitus, and hearing disorders. In uncomplicated cases affecting a single dermatome, the chief morbidity is intense, burning pain. The vesicles may become superinfected but usually resolve in 14-21 days. After the vesicular rash resolves, patients may develop postherpetic neuralgia, a common complication characterized by pain that persists for longer than 1 month. This complication is most common in patients older than 50 years, and its intensity can be incapacitating. The diagnosis is primarily based on the patient’s clinical history and physical findings. Laboratory tests (eg, Tzanck smear, direct immunofluorescence assay, polymerase chain reaction [PCR]) or viral cultures may be useful in difficult cases. The classic histologic findings are multinucleated giant cells with an accentuation of nuclear material at the periphery of the nuclei. The mainstays of treatment are antiviral therapy and analgesia. For patients with a distribution in a single dermatome, initial therapy may include nonsteroidal anti-inflammatory drugs (NSAIDs) with narcotics for analgesia. Dressings wetted with tap water or 5% aluminum acetate (Burow solution) may be applied to the affected skin for 30-60 minutes 4-6 times per day. Lotions (eg, calamine lotion) may also help relieve the discomfort. Oral antiviral therapy decreases pain, shortens the duration of the lesions, reduces the incidence of complications, and lowers the incidence of postherpetic neuralgia if it is started within 48 hours of the onset of the lesions. Some practitioners extend this window to 72 hours. Patients with disseminated zoster, multidermatomal involvement, suspected or known CNS involvement or relative immunosuppression should be treated with parenteral acyclovir and admitted to the hospital. Finally, large-controlled trials have investigated the role of steroids in combination with antiviral therapy, demonstrating improvement in the healing rate of lesions and time to resolution of acute pain. Caution should be exercised when prescribing steroids to patients with certain medical conditions (eg, diabetes mellitus, gastritis) that may be exacerbated by the side effects of this class of drugs.


Authors:

Martin I. Newman, MD, Associate Staff, Department of Plastic and Reconstructive Surgery, Cleveland Clinic Florida, Weston Margaret J. Gorensek, MD, FACP, FAAP, Department of Plastic and Reconstructive Surgery and the Department of Infectious Diseases, Cleveland Clinic Florida Rick Kulkarni, MD, Attending Physician, Director of Informatics, Department of Emergency Medicine, Olive View - UCLA Medical Center, Assistant Professor of Medicine, David Geffen School of Medicine at UCLA

References:

Chang AK. Osgood-Schlatter Disease. eMedicine journal [serial online]. February 10, 2005. Available at: www.emedicine.com/emerg/topic347.htm. Accessed November 14, 2005. Ozonoff MB. Pediatric Orthopedic Radiology. 2nd ed. Philadelphia, PA: WB Saunders 1992: 371-2. Resnick D. Diagnosis of Bone and Joint Disorders. 4th ed. Philadelphia, PA: WB Saunders; 2002: 3729-30, 3714-8. Wheeless’ Textbook of Orthopedics.2005. Data Trace Publishing Company. Available at: www.wheelessonline.com. Accessed November 14, 2005

eMedicine Editor:

Luis Lovato, MD, Attending Physician, Director of Critical Care, Department of Emergency Medicine, Olive View - UCLA Medical Center, Assistant Professor of Medicine, David Geffen School of Medicine at UCLA

Source
http://emedicine.com

Jan 2006

 
     

 

 

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